The effect of shame on prosocial behavior tendency toward a stranger.

BACKGROUND: This study aimed to examine the effect of different types of shame on prosocial behavior tendency to different help-seekers. METHODS: A total of 120 participants were randomly assigned to a neutral mood condition, a public shame or a private shame condition. RESULTS: All participants rated their willingness to help a benefactor and a stranger in an everyday helping situation and a money-donating situation after emotion-induction. The study found a higher willingness of participants in the public shame group to help strangers than those in neutral mood and private shame groups. CONCLUSION: These findings support a facilitation effect of public shame on prosocial behavior tendency toward strangers, indicating an effect of restoring motive of shame on social interaction. The results are further discussed in light of the functionalism of shame.

Lipocalin-2 participates in sepsis-induced myocardial injury by mediating lipid accumulation and mitochondrial dysfunction.

Background: Sepsis-induced cardiomyopathy (SIC) is one major cause of death for sepsis but lacks timely diagnosis and specific treatment due to unclear mechanisms. Lipocalin-2 (LCN-2) is a key regulator of lipid metabolism which has been recently proved closely related to sepsis, however, the relationship between LCN-2 and septic myocardial injury remains unknown. We aim to explore the role of LCN-2 in the pathological progress of SIC based on clinical and laboratory evidence. Methods: Consecutive patients admitted to the intensive care unit (ICU) from August 2021 to April 2022 fulfilling the criteria of severe sepsis were included. The level of LCN-2 in plasma was assayed and analyzed with clinical characteristics. Biostatistical analysis was performed for further identification and pathway enrichment. Mouse model for SIC was thereafter established, in which plasma and tissue LCN-2 levels were tested. RNA sequencing was used for verification and to reveal the possible mechanism. Mitochondrial function and intracellular lipid levels were assayed to further assess the biological effects of targeting LCN-2 in cardiomyocytes with small interference RNAs (siRNAs). Results: The level of LCN-2 in plasma was markedly higher in patients with severe sepsis and was associated with higher cardiac biomarkers and lower LVEF. In the in vivo experiment, circulating LCN-2 from plasma was found to increase in SIC mice. A higher level of LCN-2 transcription in myocardial tissue was also found in SIC and showed a clear time relationship. RNA sequencing analysis showed the level of LCN-2 was associated with several gene-sets relevant to mitochondrial function and lipid metabolism-associated pathways. The suppression of LCN-2 protected mitochondrial morphology and limited the production of ROS, as well as restored the mitochondrial membrane potential damaged by LPS. Neutral lipid staining showed prominent lipid accumulation in LPS group, which was alleviated by the treatment of siLCN2. Conclusion: The level of LCN-2 is significantly increased in SIC at both circulating and tissue levels, which is correlated with the severity of myocardial injury indicators, and may work as an early and great predictor of SIC. LCN-2 probably participates in the process of septic myocardial injury through mediating lipid accumulation and affecting mitochondrial function.

IL-13 Derived Type 2 Innate Lymphocytes Ameliorates Cardiomyocyte Apoptosis Through STAT3 Signaling Pathway.

The involvement of cardiomyopathy during sepsis means higher mortality and prolonged length of hospital stay. Many efforts have been made to alleviate the apoptosis of cardiomyocytes in sepsis. The huge potential of IL-13 in tissue repair has attracted increasing attention. In the present study, we used LPS-treated mice or primary cardiomyocytes as a sepsis model to explore the anti-apoptotic ability of IL-13. It was found that an increased level of exogenous IL-13 was beneficial to the recovery of heart function in sepsis, and this anti-apoptotic effect of IL-13 was probably through enhancing the phosphorylation of STAT3 Ser727. In addition, we identified that the heart protective effect of IL-13 was associated with type 2 innate lymphocytes (ILC2). All these findings may provide a potential promising treatment for sepsis-induced cardiomyopathy.

Engineered Biomimetic Nanoplatform Protects the Myocardium Against Ischemia/Reperfusion Injury by Inhibiting Pyroptosis.

Protection of cardiomyocytes against oxidative stress is vital to alleviate myocardial ischemia/reperfusion injury (MI/RI). However, antioxidative treatment is hampered by the lack of safe and effective therapeutics. Polydopamine (PDA), as a biodegradable class of nanomaterial with excellent antioxidant properties, has shown great potential in treating MI/RI. To achieve site-specific antioxidative efficacy, we established a PDA-based biomimetic nanoplatform (PDA@M), which consisted of a polydopamine core and a macrophage membrane shell to form a shell-core structure. By inheriting the inherent migration capability of macrophages, PDA@M was able to target the infarcted myocardium and exert an antioxidative effect to protect the myocardium. The results demonstrated that the accumulation of the membrane-wrapped nanoparticles (NPs) in the infarcted myocardium was greatly increased as compared with PDA alone, which effectively relieved the MI/RI-induced oxidative stress. PDA@M largely decreased the infarct size and improved the cardiac function post-MI/RI. Our study revealed that PDA@M could inhibit cell pyroptosis by suppressing the NLRP3/caspase-1 pathway, which is known to play a significant role in the antioxidant signaling pathway. In summary, PDA@M can target the infarcted myocardium and exert antioxidative and antipyroptosis functions to protect the myocardium against MI/RI-induced oxidative stress, suggesting that it may prove to be a potential therapeutic agent for MI/RI.